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H2O2 oxidation enhanced wild type ERK2-MEK1/2 interaction (Fig. 8B), as was previously observed in Fig. 6B.

Interestingly, studies have shown that antibodies against prM have been shown to enhance wild type DENV infection [ 37] and the levels of prM antibodies were found to be higher in patients with secondary infections compared with sera from primary DENV infections [ 38].

These results indicate that DRAM overexpression enhances wild-type p53-dependent apoptosis.

However, the mechanism of DRAM to enhance wild-type p53-dependent apoptosis remains unclear.

Next, we showed that DRAM enhanced wild-type p53-dependent apoptosis.

Unlike increased gene dosage of SIR2 in a wild-type strain (Smith et al. 1998b), NAB3 did not enhance wild-type rDNA silencing.

When wild-type p53 is expressed, the expression of the target gene DRAM increases and contributes to apoptosis induction, and more potent expression of DRAM is expected to further enhance wild-type p53-dependent apoptosis.

It has also been suggested that anti-prM antibodies could enhance wild-type DENV infection (Huang et al. 2005, 2006) and increase disease severity in infants upon primary infection (Chau et al. 2009).

Phosphorylation in RSK2 was enhanced by wild type Tat, but not TatF38A, indicating that Tat binding to RSK2 is required for the increase in kinase activity and S227 phosphorylation of RSK2 (Figure 5C).

Resistance to PMs is enhanced in wild type plants treated with JA, as well as in cev1 mutants that constitutively activate the JA pathway [ 52].

The effect of Atg6 RNAi on the reporter expression was remarkably enhanced when wild type Notch protein was coexpressed in the wing imaginal disc cells), further indicating that Notch signaling is highly activated in the lack of Atg6.